Molecular limits to natural variation

Darwin’s theory that species originate via the natural selection of natural
variation is correct in principle but wrong in numerous aspects of application.
Speciation is not the result of an unlimited naturalistic process but of an intelligently
designed system of built-in variation that is limited in scope to switching ON and
OFF permutations and combinations of the built-in components. Kirschner and Gerhart’s
facilitated variation theory provides enormous potential for rearrangement
of the built-in regulatory components but it cannot switch ON components that do
not exist. When applied to the grass family, facilitated variation theory
can account for the diversification of the whole family from a common ancestor—as
baraminologists had previously proposed—but this cannot be extended to include
all the flowering plants. Vast amounts of rapid differentiation and dispersal must
have occurred in the post-Flood era, and facilitated variation theory can
explain this. In contrast, because of genome depletion by selection and degradation
by mutation, the potential for diversification that we see in species around us
today is trivial.

Darwinian evolution

Figure 1. Potential for variation in modular regulatory control
systems. The hair dryer (A) and the vacuum duster (B)
consist of similar components, but one is wired up to blow air, the other is wired
up to suck air. The axolotl (C) is an adult salamander that has
retained its juvenile gills; if thyroxin is given at the right time, it develops
into a normal salamander (D) with lungs.

Charles Darwin will always be remembered for turning descriptive biology into a
mechanistic science. His famous 1859 book The Origin of Species by Means of Natural
Selection, or the Preservation of Favoured Races in the Struggle for Life
argued persuasively that species are not immutable creations but have arisen from
ancestral species via natural selection of natural variation. Two main points contributed
to Darwin’s success:

he presented a simple, testable, mechanical model that enabled other scientists
to engage experimentally with the otherwise overwhelming and bewildering complexity
of life;

unlike others, Darwin approached the subject from many different angles, examined
all the objections that had been raised against the theory, and provided many different
lines of circumstantial evidence that all pointed in the same direction.

He went wrong in four main areas, however. First, he proposed an entirely naturalistic1 mechanism, but we now know
that it must be intelligently designed.2
Second, he extrapolated his mechanism to all forms of life, but we will soon see
that this is not possible. Third, he went wrong in proposing that selection worked
on every tiny advantageous variation, so it led to the continual ‘improvement
of each creature in relation to its … conditions of life.’3 By implication, deleterious variations were eliminated.
We now know from population biology that selective advantages only in the order
of ≥10% have a reasonable chance of gaining fixation.4 The vast majority of mutations are too insignificant
to have any direct influence on reproductive fitness, so they are not eliminated
and they accumulate relentlessly like rust in metal machine parts. The machine can
continue to function while the rust accumulates, but there is no improvement in
the long term, only certain extinction.5

Fourth, he proposed that reproductive success—producing more surviving offspring
than competitors—was the primary driving force behind species diversification.
If this were true, then highly diversified species in groups like the vertebrates,
arthropods and flowering plants would produce more surviving offspring per unit
time than simpler forms of life. This is not generally true—quite the opposite.
The ratio of microbial offspring numbers per year compared with higher organisms
is in the order of billions to one.

Facilitated variation theory

Kirschner and Gerhart’s facilitated variation theory provides a far
better explanation of how life works. In a companion article,2 I showed that this requires an intelligent designer
to create life with the built-in ability to vary and adapt to changing conditions,
otherwise it could not survive. This leads us to the important question of the limits
to natural variation.

The limits of natural variation today are extremely narrow, being evident only at
the variety and species level. Genesis history requires a far greater capacity for
diversification in the ante-diluvian world to be available for rapidly repopulating
the Flood-destroyed Earth, and quickly restoring the ecological balances crucial
to human habitability. Baraminologists have identified created kinds that range
from Tribe (a sub-family category, e.g. Helianthus and its cousins within
the daisy family),6 to Order
(a super-family category, e.g. cetaceans—the whales and dolphins).7

Theoretical limits to natural variation

Scope for change in core structure

According to facilitated variation theory, the capacity to vary requires:

functional molecular architecture and machinery,

a modular regulatory system that maintains cellular function but provides built-in
capacity for variation through randomly rearranged circuit connections between machines
and switches,

a signaling network that coordinates everything.

Most variation occurs between generations by rearrangement of ‘Lego-block-like’
regulatory modules. Over this timescale, we can emphatically say that no change
at all occurs in the molecular architecture and machinery, because it is
physically passed in toto from mother to offspring in the egg cell.

Variation between generations must therefore be limited to the regulatory
and signaling systems.

Scope for change in regulatory modules

The law of modules2 says that the basic module of information
has to contain functionally integrated primary information plus the necessary
meta-information to implement the primary information. This information
has to be kept together so that the module retains its functionality.

Genes only operate when they are switched ON. Their default state is to remain OFF.
Genes don’t usually work alone, but as part of one or more complexes. Even
the several different exons (the protein-coding segments) within a gene
can participate in different gene complexes, some being involved with up to 33 other
exons on as many as 14 different chromosomes.8
And genes are not just linear segments of DNA, but multiple overlapping structures,
with component parts often separated by vast genomic distances.9

Sean Carroll, a leading researcher in developmental biology says, ‘animal
bodies [are] built—piece by piece, stripe by stripe, bone by bone—by
constellations of switches distributed all over the genome.’10 Evolution, he believes, occurs primarily by adding
or deleting switches for particular functions, for this is the only way to change
the organism while leaving the gene itself undamaged by mutation so that it can
continue to function normally in its many other roles. Carroll considers this concept
to be ‘perhaps the most important, most fundamental insight from evolutionary
developmental biology.’11

Diversification via Carroll’s proposed mechanism consists of rearranging the
signaling circuits that connect up genes, modules and switches, while retaining
functionality of both the modules and the organism. Carroll tells us that gene switches
are extremely complex, comparable to GPS satellite navigation devices, and easily
disabled by mutations, so if switches can be spliced into and out of regulatory
circuits, then it must happen via a cell-controlled process of natural genetic engineering
(the law of code variation2).

Regulatory areas within gene switches are hotspots for genetic change. An average
gene switch will contain several hundred nucleotides, and within this region there
will be 6 to 20 or more signature sequences. These signature sequences
are similar to credit card PIN numbers—they allow the user to operate the
bank account—and they are easy to change. The result of such change is that
different signaling molecules will then be able to operate the ‘bank account’
of natural variation.

While there is enormous potential for variation built-in to the circuitry that connects
up regulatory modules, it is signals that trigger the switches and their functional
modules.

There are about 500 or so ‘tool-kit proteins’ that are highly conserved
across all forms of life and that carry out a wide range of basic life functions.
For example, bone morphogenetic protein 5 (BMP5) regulates gastrulation
and implantation of the embryo, and the size, shape and number of various organs
including ribs, limbs, fingertips, outer ear, inner ear, vertebrae, thyroid cartilage,
nasal sinuses, sternum, kneecap, jaw, long bones and stature in humans, and comparable
processes in other animals including the beaks of Darwin’s Galápagos
finches.

The signature sequences recognized by such tool-kit proteins are usually about 6–9
nucleotides long. A 6-nucleotide sequence can have 46 = 4096 different
combinations of the nucleotides T, A, G and C, and a 9-nucleotide sequence can have
49 = 262,144 different combinations. But there are 6 to 20 or more signature
sequences that can be recognized by the 500 different tool-kit proteins, which gives
somewhere between 5006 (~1016) to 50020 (~1054)
different possible combinations.

An obvious limitation to change in regulatory circuits is that switches can only
switch ON functions that already exist. It is easy to switch OFF an existing
function, but it is impossible to switch ON a function that does not exist.

Two examples of regulatory variation are given in figure 1. The hair dryer and the
vacuum duster both use similar materials—motorized fan, plastic housing, power
circuit and switch. In one, the control circuit is wired up to blow air;
in the other, the circuit is reversed, and the machine sucks air. A biological
example is the axolotl, a salamander that has retained its juvenile gills
into adulthood. This can happen if there is an iodine deficiency in the diet, or
if a mutation disables thyroxin production. By adding thyroxin, the axolotl will
develop into a normal salamander. Both these switch-and-circuit rearrangements seem
to be simple changes, but they are possible only because complex mechanisms of operation
already exist within the system.

Scope for change in signaling networks

While there is enormous potential for variation built-in to the circuitry that connects
up regulatory modules, it is signals that trigger the switches and their
functional modules. What scope is there for diversification in signal networks?

Signal networks are compartmented. They operate as a cascade within each
compartment—one signal triggers other signals, which trigger other signals
etc. Each compartment cooperates with its adjacent compartments so that the unity
and functionality of the organism is maintained, but they do not influence activities
beyond their local neighbourhood.

Figure 2. Embryonic switching cascades represented as a ‘domino
cascade’. The domino cascade is set up on the left so that when the ‘Start’
domino is toppled, the sequential falling of dominoes will trigger the next activity
in the series, but also trigger other developmental modules in the outer circles,
until the ‘Stop button’ is hit. Once the cascade is complete, an organism
does not need any of the sequence again so it is permanently shut down, as on the
right where all the dominoes have fallen and will not get up again. There is no
coded information in this signal network because everything that has to be done
has been designed into the pattern of dominoes. With no coded information, no mutations
or recombinations can occur, so this kind of signal network probably marks a limit
to natural variation.

The two examples I used to illustrate this point in the companion article ‘How
Life Works’2 were the propagation of plants from cell culture,
and the regeneration of double-headed and double-tailed planarian flatworms. In
both these cases, a single signal molecule triggered a dramatic developmental cascade
(shoot/root growth in the former, and head/tail growth in the latter) that was completely
independent of, but cooperative with, the other half of the whole organism.

Some signals are hard-wired into the cell, while others are soft-wired. An example
of a hard-wired signal occurs within the apoptosis cascade for dismantling
cells and recycling their parts. In a normal cell, apoptosis is extensively integrated
with a wide range of functional systems and can be triggered by a variety of causes
through a complex signaling network. However, in human blood platelets
the system is isolated from its normal whole-cell environment and we can see it
operating in a much simpler form.

A complex of two proteins, Bcl-xL and Bak, performs the function
of a molecular switch. When Bcl-xL breaks down, Bak triggers cell-death.12 In a normal whole cell,
homeostasis maintains the balance between Bcl-xL and Bak, but
platelets are formed by the shedding of fragments from blood cells and there are
no nuclei in them. Once the platelets are isolated from homeostatic control, Bcl-xL
breaks down faster than Bak, so the complex provides a molecular clock
that determines platelet life span—usually about a week. No signal is sent
or received in this hard-wired system, so there is no room for diversification.

Hard-wired signaling networks are probably a major component of stasis. We can visualize
them by using a domino cascade model, illustrated in figure 2. In this case, embryogenesis
is symbolized as a series of events in the main circle, which trigger other peripheral
cascades as they proceed. Each cascade continues until it meets a STOP signal, at
which point the whole circuit is shut down. A similar thing happens in individual
cells when they differentiate. Embryonic stem cells have the potential to become
any cell in the body, but once the cascade is traversed, all options but one are
shut down.

In contrast, a soft-wired system sends actual signal molecules, raising the possibility
of adaptive change—e.g. sending a different signal molecule. A recent study
of red blood cells investigated cell fate decision making—whether to proliferate,
to kill themselves or to call for help. This decision lies at the very heart of
homeostasis because it determines the robustness and stability of the organism in
the face of change and challenge.

The researchers discovered that they did not need to know the detailed structure
of the decision-making system, just a knowledge of its network of signaling interactions
was sufficient to identify which components were the most important.13 This finding was confirmed in another study in
which a wide range of perturbations were applied to white blood cells and the effect
upon the cell fate decision was examined. The decision came not from any particular
target of perturbation, but as an integrated response from many different nodes
of interaction in the signaling network. The authors suggested that computations
were carried out within each node of the signaling network and the combination of
all these computations determined what the level of response should be from any
particular perturbation.14

Does this indicate a potential for adaptive change? Or does it suggest a system
that is designed to resist change?

The primary role of the signaling system is to coordinate everything towards the
goal of survival. Life can survive only by maintaining a balance between contradictory
objectives. On the one hand, it has to achieve remarkable results as accurately
as possible—e.g. plants turning sunlight into food without the high energies
involved killing the cell. On the other hand, it has to do it in an error-tolerant
and constantly variable manner to maintain its adaptive potential and its
robustness and stability.

The solution to this dilemma is error minimization. All possible routes will involve
risks of error, but the optimal solution will minimize those risks. A computer simulation
study of regulatory networks found that using an error minimization strategy leads
to the formation of control motifs (gene switching patterns) that are widely found
in very different kinds of organisms and metabolic settings.15 When applied to the ‘noise’ in yeast
gene expression that results from the ON/OFF nature of signaling, it was found to
also be the case in real life. Genes that were essential to survival exhibited the
lowest expression-noise levels when compared with genes that were not directly essential.
The author concluded that ‘there has probably been widespread selection to
minimize noise in [essential] gene expression.’ But there is a down side—noise
minimization probably limits adaptability.16

Figure 4. The grass inflorescence consists of (A)
the basic unit of a single terminal flower (spikelet) on a short stalk (pedicel)
which is repeated in a terminal group of branches (B). This terminal
group structure is then repeated on side branches (C), with the
lower branch(es) including further internal branching. This basic inflorescence
type is called a panicle.

Since the goal of signal coordination is survival, I suspect that the large, interconnected
signaling networks in all forms of life contribute more to stasis than to change.

Practical limits to natural variation

It is impossible to describe the full range of natural variation across all life
forms in a journal article, so I will focus just on variation within the grass family
(Poaceae), and between it and other families of flowering plants (Angiosperms).

The grass family comprises about 10,000 species in about 700 genera. Is it possible
that maize, lawn grass and bamboo all arose from a common ancestor? Baraminologists
believe so.17

Grass morphology

The easiest way for us to conceptualize the extent of natural variation is through
illustrations of morphological variations. We need to keep in mind that much more
than morphological variation is involved in speciation, but it can serve as a convenient
surrogate for our present purpose. The basic structure of a generalized grass flower
(spikelet) is illustrated in figure 3.

Figure 5. Ordination and classification of specimens of the three
native Puccinellia species identified in Western Australia, based on 34
morphological characters. Principle Coordinates 1 and 2 provide a 2-dimensional
representation of the differences between the specimens and a clustering algorithm
identified groups of similar specimens (ellipses).

A common variation on the standard structure is the development of an awn upon the
apex of the lemma (or glume) in figure 1C. This transformation is fairly straightforward.
The apex of the lemma is extended into a long straight awn, then a regulatory change
causes the edges to grow faster than the centre, which causes the base part of the
awn to spiral around into a twisted column, leaving a straight or curved
bristle at the top.

Grasses generally have a multitude of spikelets, arranged into a terminal structure
called the inflorescence, as shown in figure 4.

Species-level variation in the Australian salt grass Puccinellia

Salt grasses of the genus Puccinellia are distributed worldwide, from the
Antarctic to the Arctic, and they occur right across southern Australasia (Australia
and New Zealand) in marine salt marshes, around the edges of inland salt lakes and
on salinised pasture lands. They have a quite generalized grass morphology, with
no special adaptations for dispersal, as many other grasses do, so they may represent
a typical primordial grass.

The most widespread species, found right across Australasia, is Puccinellia stricta.
When Edgar18 described
the New Zealand species in 1996 she noted some differences between Australian and
New Zealand populations of P. stricta and suggested that further detailed
study was warranted. I was fortunately able to undertake that study,19 with results that are quite typical of many widespread
plant genera. My study focused on the genus in Western Australia (WA), where three
native species were identified—P. stricta, P. vassica and P. longior.
An ordination and classification of specimens based on their morphological characteristics
is shown in figure 5.

Figure 6. Ordination and classification of specimens of Puccinellia
stricta from across Australasia. The group labeled perlaxa had
been identified as a subspecies of P. stricta. Four geographically isolated
regions were sampled: WA = Western Australia, SE Aus
= South East Australia (Victoria, South Australia and New South Wales), Tas
= Tasmania, NZ = New Zealand. The axes of ordination and the ellipses
of classification have the same meaning as Figure 3 and were based on the same 34
morphological characters.

The plot shows that all three species are well separated from one another, with
members of each species being more closely similar to members of their own species
than to other species.

I then needed to know how our specimens of Puccinellia stricta compared
to specimens of the same species from right across Australasia. Loan specimens were
obtained from other herbaria and the same analysis was carried out as for the WA
specimens. A very different plot resulted, as shown in figure 6.

In this case, a new species was clearly separated out from the rest, while the remainder
spread broadly right across the ordination space. The group labeled perlaxa
(occurring only in southeast Australia) had previously been identified as a subspecies
of stricta, but from this analysis it was clear that it warranted species
status, so we named it Puccinellia perlaxa.

The big picture of the native Australasian species of Puccinellia that
emerged from this study was of a single widespread species, P. stricta,
that varied in a continuous manner right across the whole region, and then localized
species with restricted distributions that could generally be explained in terms
of local ecological and/or geographical factors.

Historically, therefore, it is most likely that the widespread species was the progenitor
of the all the other species. It has retained at least some of its capacity for
variation, and certainly a greater capacity (wider dispersion in the ordination
space) than any of the other species that I studied.

Morphological variation in Australian Puccinellia

Figure 7. Panicle variations within Australian species of Puccinellia.
The contracted panicle with a variety of branch lengths at A is
typical. B has numerous spikelets crowded along very short branches,
while C has very few spikelets on very short branches, and
D has few spikelets that are mainly on the ends of very long branches.
Images were scanned from dried herbarium specimens; in life, D
would have had straight branches and a more symmetrical shape.

Figure 8. Variations in upper glume length (marked with black bars)
in spikelets of some Australian species of Puccinellia.

Figure 9. Paleas from five different Australian species of Puccinellia.
Note the variation in hair development on the margins, ranging from glabrous (no
hairs) on D, a few hairs near the apex of E, the top half of B with hairs and the
lower region glabrous, with A and C having hairs extending into the lower half.

Figure 10. Retrogression of Panicoid grass spikelets. The characteristic
condition in the Tribe is to have one terminal fertile floret subtended by one sterile
floret. The primordial condition at A has the sterile floret male. Condition B has
lost the anthers of the sterile floret. Condition C has lost the palea of the sterile
floret. Condition D has lost the lower glume. The series E, F, G and H illustrate
the same pattern of retrogression but with the spikelet axis rotated in relation
to its adjoining branch.

Figure 11. Transformation of a panicle into wheat. The side branches
of A are eliminated to give B, the number of spikelets
is increased to form C, then the pedicels are reduced to form
D.

Australian Puccinellia species vary most markedly in their panicle structure,
a few of which are illustrated in figure 7.

Puccinellias have multiple florets per spikelet, ranging from 3 or 4 up to 10 or
more. One feature that varies significantly in spikelet structure is the length
of the upper glume, illustrated in figure 8.

The palea also varies significantly, particularly in the extent of hairs on the
margins, as shown in figure 9.

Genus-level variations in Tribe Paniceae

The grass family is divided up into Tribes of genera that (ideally) reflect their
common ancestry. The largest Tribe is Paniceae, and Häfliger and Scholz have
suggested that the spikelet variations within this Tribe follow a fairly simple
pattern of retrogression from the original Paniceae spikelet,20 as illustrated in figure 10.

Sub-family variation within Poaceae

Argentinian researchers Vegetti and Anton have shown that if we begin with a panicle
as the primordial grass inflorescence, then every other generic form can be derived
simply by adding, subtracting, shortening or lengthening the components of the panicle.21 I will take just three
types of transformations that represent different sub-family groups within Poaceae—wheat,
maize and silkyhead lemon grass.

Wheat

The hypothesized transformation of a panicle structure into the reduced seedhead
of a wheat plant via the Vegetti-Anton theory is illustrated in figure 11.

Maize

Figure 12. Transformation of a panicle into maize. The middle branches
of the panicle A are replaced with leaves and leafy bracts, and
the lower branches are transformed into a spike (like wheat, Figure 9) to form
B. The upper spikelets lose their female parts, and the lateral spikelets
lose their male parts to form C. The male spikelets multiply, and
the female spikelets elongate their pollen receptors to form a tassel that emerges
from the enveloping leafy bracts, to form D.

Transformation of a panicle into the compact seedhead of maize is more complex,
but still conceivable, as illustrated in figure 12. The primordial panicle could
have been divided by the panicle branches being switched OFF in the mid-section,
and leaf modules being turned ON. A leaf within the inflorescence is called a ‘spathe’
leaf. Apical dominance is a common mechanism in all plants for repressing growth
below the apex until conditions are appropriate. This normally controls the proliferation
of fertile seeds within grass spikelets. It represses female organ development more
strongly than the male parts, so in many grasses the apical florets within a spikelet
will be either male or sterile, and only the lower florets (those furthest away
from the dominating apex) will produce fertile seed. This mechanism is already in
place to suppress female organ development in the top branches of the maize plant,
making them all male. But the lower branches of the inflorescence are now far distant
from the apex, so apical dominance is eliminated and the female organs grow uninhibitedly,
perhaps out-competing the male organs and suppressing them altogether. Leaf and
bract growth in the lower parts is stimulated and they cover the female spike entirely.
This causes the female florets to lengthen their pollen receptors so that they can
reach the open air and receive wind-dispersed pollen, making the silky tassel at
the end of a corn-cob.

Silkyhead lemon grass

Figure 13. Transformation of a primordial panicle into the spatheate
panicle of Cymbopogon obtectus. The branching pattern in A
is reduced to a repeating set of branches in which a sessile fertile spikelet with
an awn occurs at each secondary branch point, accompanied by a pedicellate awnless
sterile spikelet (B). Pairs of these branched structures are subtended
by a spathe leaf, from which they emerge at flowering time (C)
to produce the complex mature panicle (D).

Transformation of the panicle into silkyhead lemon grass (Cymbopogon obtectus)
can be hypothesized by reducing the pedicel of alternate spikelets so that they
occur in pairs—one pedicellate, the other sessile. The pedicellate spikelet
retains apical dominance and is sterile or male, and the sessile spikelet is fully
fertile, but it also develops an awn on its lemma (see figure 3). The paired branching
structures occur also in pairs, and a leaf growth module is switched ON within the
developing inflorescence to produce a spathe leaf surrounding each pair of branched
structures. Hairs are normally present in many parts of the inflorescence, and are
usually short, but in Cymbopogon obtectus, the hairs are abundant and long,
producing a fluffy white ‘silkyhead’ at flowering time, as illustrated
in figure 13.

Origin of the angiosperms

Within the grass family, diversification from a common ancestor seems to be fairly
straightforward, and could have occurred via numerous rearrangements of parts that
were already present in the primordial grass ancestor. But can we continue this
process back to a common ancestor with daisies, orchids and all other flowering
plants?

Recent discoveries of fossil flowers show that angiosperms were already well diversified
when they first appeared in the fossil record.

A recent review of the subject was entitled ‘After a dozen years of progress
the origin of angiosperms is still a great mystery.’22 The ‘progress’ referred to was the
enormous effort put into DNA sequence comparisons, in the belief that it would give
us the ‘true’ story of life’s origin and history. While such comparisons
have proved of great value in sorting out species and genus relationships, the results
for family relationships and origin of the angiosperms has often been confusing
and/or contradictory—thus the remaining ‘mystery’.

Recent discoveries of fossil flowers show that angiosperms were already well diversified
when they first appeared in the fossil record. The ‘anthophyte theory’
of origin, the dominant concept of the 1980s and 1990s, has been eclipsed by new
information. Gnetales (e.g. Ephedra, from which we get ephedrine), previously
thought to be closest to the angiosperms, are now most closely related to pine trees.
To fill the void, new theories of flower origins have had to be developed, and ‘Identification
of fossils with morphologies that convincingly place them close to angiosperms could
still revolutionize understanding of angiosperm origins.’22

Conclusions

In contrast to Darwin’s proposed slow development of variation, the evidence
supports a vast amount of rapid differentiation in the past, degenerating into only
trivial variations today—a far better fit to Kirschner–Gerhart theory
and Genesis history.

Theoretically, the greatest scope for natural variation appears to lie in the almost
infinite possible permutations of the Kirschner–Gerhart ‘Lego-block’
regulatory module combinations, and these could rapidly produce the enormous diversification
implied by Genesis history. In contrast, there is no scope at all for change in
the machinery of life from one generation to the next because it is passed on in
toto from the mother in the egg cell. Signaling networks appear to be limited
in their scope for diversification, particularly those that are hard-wired (designed
into the system) into compartments and cascades that have symmetry and functional
constraints. The elaborately interconnected signaling networks are very robust in
the face of perturbation, and provide a crucial component of stasis. There is some
potential for variation in the signaling molecules that are sent, but error minimization
limits its functional scope.

From a practical point of view, diversification of the whole grass family from a
common ancestor is conceptually feasible via switching ON and OFF the original component
structures within a primordial grass. It is not possible to switch ON components
that don’t exist, however, so this mechanism cannot be extrapolated to include
a common ancestor between grasses and other angiosperms such as daisies and orchids.

Flowering plants display an enormous amount of differentiation and dispersal (between
250,000 and 400,000 species in 400 to 500 families worldwide) and appear only in
the upper levels of the fossil record. Most of this diversification appears therefore
to have happened rapidly, possibly in the post-Flood era. A possible reason for
this is that the flowering plants were originally planted in the Garden of Eden
and radiated worldwide mainly after the Flood.23

This is not Darwinian evolution. It is intelligently designed, built-in potential
for variation in the face of anticipated environmental challenge and change. The
word ‘evolution’ is still useful in describing processes of historical
diversification, but its Darwinian component is now only a minor feature. In contrast
to Darwin’s proposed slow development of variation, the evidence supports
a vast amount of rapid differentiation in the past, degenerating into only
trivial variations today—a far better fit to Kirschner–Gerhart theory
and Genesis history.

Acknowledgments

I am grateful for the comments from three referees and numerous colleagues, which have helped to improve this article.

Recommended Resources

People are told: ‘Evolution is happening all around us!’ This superb
presentation shows clearly that the examples used are actually the opposite of what
would support evolution. Both natural selection and mutation fit beautifully within
a biblical framework and are powerful tools to defend Genesis. (High School–Adult)
60 mins. Includes English sub-titles and a 3-minute CMI promotional segment.

Author: Dr J.C Sanford This landmark book presents powerful evidence for creation.
The author, a well-known ex Cornell University professor of genetics, shows how
mutations and natural selection do not account for the information in the human
genome. 3rd edition. (High School–Adult) 229 pages.

Startling data from recent creation—in our DNA.. One of the world’s foremost experts
on genetics traces the history of human genetic decline due to mutations in our
DNA. The evidence is startling to those who don’t believe in the Genesis account
of Creation because it refutes conventional dates for alleged human evolution. This
is powerful evidence for the Bible’s timescale for human history. (High School–Adult)
49min.

References

Darwin mentioned a Creator on the last page of The Origin,
but later regretted it, acknowledging it was only a concession to public opinion.
Private letter from C. Darwin to J. D. Hooker, Down, Friday night (17 April 1863),
<darwin-online.org.uk/content/frameset?viewtype=side&itemID=F1452.3&pageseq=30>,
23 May 2008. Return to text.

Darwin, C.R., The origin of species by means of natural selection,
or the preservation of favoured races in the struggle for life, John Murray, London,
6th ed., Summary of Chapter IV, 1872. Return to text.

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